Antibiotics are medicines that help your body fight bacteria and viruses,
either by directly killing the offending bugs or by weakening them so that
your own immune system can fight and kill them more easily. The vast
majority of antibiotics are bacteria fighters; although there are millions
of viruses, we only have antibiotics for half-a-dozen or so of them.
Bacteria, on the other hand, are more complex (while viruses must "live"
in a "host" (us), bacteria can live independently) and so are easier to kill.

(A note for the purists out there: strictly speaking, an "antibiotic" is
a bacteria-fighting medicine that is derived from a biological source
(plant, mold, or other bacteria). Since most people use the term
"antibiotic" for any anti-infection medicine, I am doing the
same here.)

Bacteria (and viruses) aren't particularly intelligent. However, it is
possible -- and unfortunately all too common -- for bacteria and some viruses
to "learn" how to survive even with antibiotics around.

There are several ways that bacteria can become resistant. All of them involve
changes in the bacteria's genes.

Bacterial genes mutate (change), just like the genes of larger
organisms (including humans) mutate. Some of these changes happen because
of chemical or radiation exposure; some just happen randomly, and no one's
sure quite why. If bacteria with a changed gene is less susceptible to
an antibiotic, and that antibiotic is around, the less susceptible (and
more resistant) version of the bacteria is more likely to survive the
antibiotic and continue to multiply. This is particularly likely to
happen if the amount of antibiotic around isn't quite enough to kill all
of the bacteria quickly -- as can happen if you don't take enough of the
antibiotic to keep its level in your body high, or if you stop taking the
antibiotic too early. This is why when you are prescribed an
antibiotic you MUST take it exactly as prescribed, and for as long as it
was prescribed: you may feel better after only a short time,
but you may still have some bacteria left in you -- not enough to make
you feel bad, but enough to come back -- and those bacteria left include
the ones that are partly resistant to the antibiotic already and likely
to become more resistant. It's also why we don't (or shouldn't) give
you an antibiotic for an illness like a cold that isn't likely to be
bacterial: the antibiotic will kill off susceptible bacteria, leaving
bacteria that are resistant to that antibiotic and which can cause a
later infection -- and one that won't respond to the previous
antibiotic.

Although there are many different species of bacteria, some bacteria can
"trade" genes with other bacteria. If you have a relatively harmless
bacteria in you -- say, in your mouth or your intestines (both places are
chock full of bacteria) -- and you've used (or overused or misused)
antibiotics some of those harmless bacteria will become resistant to the
antibiotics you've (over-, mis-)used. They can then give the resistance
genes they have developed to other, harmful bacteria.

There are viruses around that attack bacteria rather than plants, animals,
or people. Most of these viruses just kill the bacteria, but sometimes
the viruses can copy genes -- like the antibiotic resistance genes -- from
one kind of bacteria to another.

Human and animal viruses can also develop resistance to antiviral antibiotics,
usually through mutation. This isn't a big issue, since there aren't a lot of
antiviral antibiotics. However, antiviral resistance has become a major
problem in HIV (AIDS) therapy, where the virus rapidly becomes resistant to
the first-line antivirals such as AZT. Resistance develops
particularly fast in patients who do not take their medicines properly, and in
those whose immune systems can't help clean up after the antibiotics. This is
one reason why tuberculosis (which is caused by a bacteria that multiplies
very slowly and that is specifcally fought by the part of the immune system
that HIV disables) has resurged since the appearance of AIDS.

There are now so many different antibiotics on the market that it's hard
for us to keep track of them all. Personally, I almost always look up
the dose of an antibiotic when I prescribe it, just to make sure that I'm
giving the right medicine in the right dose. I also tend to stick to a
few antibiotics in my practice, so that I can stay familiar with their
effects and side-effects; most pediatricians I know do the same.

In the early 20th century, Alexander Fleming discovered that
a mold called Penicillium (the cells are pencil-shaped
when you look at them under a microscope) produces chemicals which kills
most of the bacteria nearby. (The mold is green when it grows in large
amounts, and is often found on bread. This, however, does not
mean that eating moldy bread will cure your ear ache -- or anything else.
Molds produce other things, too...) He was able to isolate
these chemicals, which are now known as "penicillins". Sometime later,
another mold was found which produced a bacteria-killing chemical, and
this chemical's molecule was found to be very similar to the penicillin
molecule; this chemical and its cousins were called "cephalosporins"
after the mold it came from. The majority of antibiotics are either
penicillins or cephalosporins; chemical changes have been made
to the molecules over the years to improve their bacteria-fighting
abilities and to help them overcome breakdown and "immunity" of
resistant bacteria.

Most bacterial cells have double layers on their outside. The outermost
layer -- the "cell wall" -- is similar to the outer layer of plant cells,
but is missing in human and animal cells. This wall must grow along
with the cell, or the growing cell will eventually become too big for
the wall and burst and die. Penicillins and cephalosporins kill
bacteria by messing up the wall-building system. Since we don't have
cell walls, and plants have a different wall-building system, neither
we, nor animals, nor plants are affected by the medicine.

There are a very few bacteria that don't have cell walls, either.
These bugs are immune to penicillins and cephalosporins for the same
reasons we are. Most bacteria do have cell walls, but many have
changed their wall-building systems so that penicillins can't interfere,
or have come up with ways to break down the medicines before the
medicines can work. When we first started using penicillin in the
40's and 50's, most bacteria could be killed by plain penicillin.
Now, because we have used penicillins and cephalosporins so often
(and, in many cases, when we really shouldn't have), there are many
bacteria that can't be killed any more by plain penicillin or even
by the "super-penicillins" and "super-cephalosporins".

Penicillins and cephalosporins usually don't cause many problems
for a patient. Like all antibiotics, they can cause mild side
effects like diarrhea. Less common side effects include rashes
(which may or may not imply a true allergy) and hives (which usually
means you're allergic to the medicine). The rarest -- and scariest --
side effect is "anaphylactic" allergy, in which your airway swells up
when you take a dose of the medicine, sometimes to the point where
you can't breathe. Although the reaction can be treated if you are
close to help, the safest thing if you are that allergic to the medicine
is never to take it at all. (In cases where you have an anaphylactic
allergy to penicillin or cephalosporins and must have it to
treat an infection, doctors can "desensitize" you temporarily, using
very small doses that are given frequently and in increasing amounts.
That is almost always done in a hospital.)

Erythromycin is another antibacterial produced by a mold. There are
a couple of new relatives of erythromycin (azithromycin and clarithromycin)
that work the same way, but kill more bugs and have slightly fewer
side effects. The erythromycin-like antibiotics are also known as
macrolides.

Erythromycin works by blocking the bacterial cell's machinery for making new
proteins. Since proteins both make up much of the cell's structure and make
the enzymes that direct all the cell's chemical reactions, blocking protein
manufacturing makes the cell unable to function. Erythromycin in low doses
will stop bacteria from growing and multiplying, but you need a higher
concentration to kill the bacteria. However, if you can stop growth until
your immune system kicks in, that will help you get rid of the infection.

Since all protein making is affected, erythromycin can slow down or
kill any bacteria, even those without cell walls. Because of this,
we use the erythromycins for several diseases, including bacterial
bronchitis, chlamydia, and
whooping cough, that penicillins and cephalosporins can't touch.

Erythromycin and its cousins don't have anything like the allergy
problems we see with the penicillins and cephalosporins, although
there are rare people who have reactions to it. The biggest problem
with these medicines is that they can irritate the stomach. I have
seen one patient who ended up with bleeding stomach ulcers after taking
erythromycin; this irritation seems to happen most often when someone
tries to take the medicine on an empty stomach. Always take
erythromycin with food or milk. (The same goes for clarithromycin.
Azithromycin doesn't irritate the stomach nearly as much as the others.)
Another problem with erythromycin -- but not with azithromycin --
is that it may cause enlargement of the pylorus, the muscle that
serves as the valve at the outlet of the stomach -- in infants. This
condition is known as
pyloric stenosis,
and is a surgical emergency if it occurs since nothing can leave the
stomach properly. In the past we treated infants with erythromycin
if they developed
whooping cough.
We now use azithromycin, which works just as well as erythromycin but
doesn't affect the pylorus (and needs to be given for only five days;
you need 14 days of erythromycin for complete treatment of whooping cough).

The sulfas (more properly "sulfanilamides" or "sulfonamides") were
the first antibiotics to be developed; they are actually completely
man-made. They interfere with certain "manufacturing" systems in
the bacterial cell, including ones that bacteria use to produce
new DNA for new bacteria. Sulfas can stop bacteria from growing,
but they cannot actually kill the bacteria.

When they were first used, sulfas worked against many kinds of bacteria.
Unfortunately, as with penicillin, the more we used the sulfas the
more bacteria became resistant to it. Sulfas also have a tendency to
produce allergic reactions -- different than those we see with the
penicillins, for the most part, but including some that are rare but
life-threatening. Because of this we don't use sulfas nearly as much
we used to, and most often when we use sulfas it's in combination with
another drug which attacks a different part of the bacteria (an attack
on two fronts is usually better than an attack on one). The drugs
we usually combine with sulfas are either erythromycin or "trimethoprim"
(see below); these combinations usually can kill bacteria rather than
just slowing them down. One frequent use of "plain" sulfas is in
antibiotic eyedrops used for conjunctivitis
("pink eye").

Trimethoprim (TMP) is another man-made antibiotic. Like the sulfas,
trimethoprim blocks an important step in the bacteria's system for
making new DNA -- but it's a different step. By itself, TMP can kill
bacteria, but very slowly. Usually, though, we use TMP in combination
with sulfamethoxazole (SMX), and the combination of TMP and a sulfa
kills bugs better. In fact, bacteria that are partly resistant to
either TMP or SMX can still be killed by the combination of the two.
The side effects of the combination are the same as those of the two
separate components.

Nitrofurantoin is another synthetic antibiotic, used mainly for
urinary tract infections.
(Since it is excreted in the urine, it concentrates in the bladder
very nicely.) Nitrofurantoin stops bacteria from growing, and can
kill bacteria with a high enough level, by blocking the bacteria's
ability to use energy it makes by "digesting" nutrients like sugar,
and by blocking other chemical reactions that use the same system.
It is not usually used for infections other than UTIs, and there
are several side effects (ranging from stomach upset to (very rarely)
malfunctioning nerves) which limit its use.

The aminoglycosides are drugs which stop bacteria from making proteins;
they work by attaching permanently to the protein machinery. Since
they attach permanently, the bacterial cell will die if it gets enough
of the drug. They can be used by themselves, or along with
penicillins or cephalosporins to
give a two-pronged attack on the bacteria.

Aminoglycosides work quite well, but bacteria can become resistant to them.
The drawbacks are large, though. Since aminoglycosides are broken down
easily in the stomach, they can't be given by mouth and must be injected or
given IV (although we can use them as eyedrops for
"pink eye"). When injected,
their side effects include possible damage (temporary or permanent) to the
ears and to the kidneys; this can be minimized by checking the amount of the
drug in the blood and adjusting the dose so that there is enough drug to kill
bacteria but not too much of it. Generally, aminoglycosides are given for
short time periods, and in the hospital where we can check both the drug
levels and the bacteria's sensitivity easily.

The quinolones, of which the best known is ciprofloxacin (Cipro&reg:),
interfere with an enzyme called DNA gyrase that is essential for duplication
of bacterial DNA. (Bacteria have only one long chromosome (DNA molecule);
the chromosome gets twisted during replication, like a telephone cord, and,
again like the telephone cord, the chromosome can become so twisted that
nothing more can be done with it. DNA gyrase is the "untwisting" enzyme.)
This interference is completely different from the interference of other
antibiotics with bacterial "machinery", and so bacteria that are resistant
to other antibiotics may be sensitive to the quinolones.

However, bacteria can develop resistance to the quinolones, too. Also,
researchers have noticed that young animals given quinolones can have damage
to their cartilage (the hard but slippery material that connects some bones
and covers the slding surfaces of joints). In the past we have avoided using
quinilones in children because of this finding, but we sometimes have to give
some children quinolones when there is no alternative antibiotic available.

Polymyxin B is an antibacterial that is produced by another bacteria. (We
usually take our antibiotics wherever we can find them...) It kills bacteria
by damaging the cell wall chemically -- just the way
soap does. It can't be taken internally, but it's very useful for skin
infections (it's part of "Polysporin") and for conjunctivitis
("pink eye").

Tetracyclines are yet another family of antibiotics oringinally found in
bacteria. They also block the protein-making machinery of certain bacteria.
One of the tetracyclines, doxycycline, is often used to treat certain
sexually transmitted diseases (such as chlamydia and gonorrhea) in older
patients. One known side effect of the tetracyclines is that they affect
development of bone and of tooth enamel in young children, and because of
this we do not usually give tetracyclines to children under age 8 years.
However, tetracycline may be the best antibiotic for some life-threatening
infections, such as
cholera and anthrax, and in such cases we may use tetracycline to treat
a young child (tetracycline often leaves a permanent brown stain on
developing teeth, but that's better than death...).

Some microorganisms, known as fungi (fungus in the singular),
are cells that are biologically more similar to animal cells than to
bacteria. Since many of the antibacterial antibiotics take advantage of
the difference between bacterial cells and animal cells, the fungi's
similarlity to animal cells makes them immune to the antibacterial
antibiotics. However, there are antibiotics available for fungi such
as Candida.
These include nystatin, the azoles (including fluconazole,
ketoconazole, and similar antibiotics), and amphotericin B. These
work by disrupting the fungal cells' machinery. Some of these antibiotics
may be applied to the skin or taken by mouth, while others must be given
IV.

Since viruses can't live outside the person or animal they infect, they are
much harder to kill off. Our immune system can find and kill many of the
viruses that attack us, but sometimes a virus can multiply and overwhelm the
immune system before the immune system "comes up to full speed". We
immunize or vaccinate
people against diseases -- mostly viral, but some bacterial -- so that their
immune systems do have that head start. That seems to be the most succesful
way to kill viruses permanently. An example is smallpox, which has been
eradicated due mainly to the use of vaccines against it -- without which the
virus killed thousands, if not millions, in epidemics. Some viruses, such as
HIV (which specifically attacks the immune system), are very hard to become
immune to, but a great deal of research is being aimed at producing a working
vaccine for those diseases.

Unfortunately, since viruses are completely dormant outside a "host" (an
infected human or animal), they can't be attacked biologically unless they
infect someone. The immune system can't go after the virus unless it's in
the body, and all of the antiviral medicines we have work only when the virus
is trying to reproduce in the body. We can destroy viruses in the environment
if we know they are there (an example is using household bleach to kill HIV
that might be on equipment contaminated with body fluids -- but bleach won't
kill HIV in the body, even if we could get it into the body safely).
Once the virus is in the body, however, all we can do is let the immune system
do its work, and in very rare cases (perhaps half-a-dozen viruses at most)
give drugs that slow down the infection so that the body can clear it out
more easily.

One often-used antiviral medicine is acyclovir; ganciclovir
and valciclovir are similar to acyclovir. These medicines slow
down infections with viruses of a certain family, which include both
varicella (chickenpox and
shingles) and the herpes viruses. Acyclovir slows down the virus'
multiplication and therefore slows down the infection. The problem is that
the varicella and herpes viruses are never actually eradicated -- they stay
in the body forever, and "reactivate" later (sometimes years later). The
recurrent sores of herpes, and the appearance of shingles years after you
have chickenpox, are examples of reactivation, and although acyclovir can
help you get over the reactivation infection, it can't actually get rid of
the viruses.

Another very well-known antiviral is triazidothymidine, better known
as zidovudine or AZT. This drug, and others like it, are used
to inhibit an enzyme called "reverse transcriptase" which HIV uses to "copy"
its own genes into the genes of the cells it infects. Once the HIV genes
are copied, the infected cell and all its offspring can produce more HIV.
(This is why an AIDS patient cannot actually get rid of all of the virus once
infected: the virus may lie dormant as inactive genes for months or years,
and the anti-AIDS drugs cannot get to the gene copies.) Like bacteria,
viruses can mutate, changing their structure so that drugs that used to work
no longer help; this explains why AZT and other reverse-transcriptase
inhibitors eventually lose their effectiveness in many patients.

A newer class of anti-AIDS drugs, the protease inhibitors, work by
blocking a different HIV enzyme. HIV uses reverse transcriptase to copy its
genes into the cell it's infecting; it uses "protease" (an enzyme that breaks
down protein) to get into the cell in the first place. Many people with AIDS
have been able to eliminate the virus from their bloodstream -- or almost
eliminate it -- by using both reverse-transcriptase inhibitors and protease
inhibitors at the same time. However, since the virus has copied itself into
cells where neither kind of drug can attack it, a patient must keep taking
the drugs forever to keep the virus from reactivating.

Note, by the way, that the antiviral drugs, even more than the
antibacterials, are tailored to the kind of viruses they are intended to
attack. AZT won't do anything for a cold, and neither will acyclovir. In
fact, there are -- so far -- no antivirals that will do anything for
the common cold. And, since there are many different viruses in several
different families that can cause colds, we are not likely to have any
anti-common-cold drugs in the near future.

Since most colds are
due to viruses attacking the mucus membranes of the nose and throat, the
only way to get over the cold is to wait for your immune system to get rid
of the virus, and for your body to produce a new, virus-free mucus membrane
surface. Resurfacing the mucus membranes takes 3-4 days (you automatically
resurface the membranes every 3-4 days), but getting rid of the virus takes a
week or two, and until the virus is gone the new membranes will keep getting
infected. Since we have no medicines that will slow down the cold viruses,
we can't do anything to speed up this process. Antibacterial antibiotics will
do nothing to help get rid of the virus, and giving
antibacterial antibiotics when there is a viral cold will likely do nothing
except help the bacteria in the nose and throat become resistant -- which
makes the next bacterial infection much harder to treat. I never give
antibiotics to someone who has only a cold, unless there seems to me to be a
very good chance that he or she may develop a bacterial infection on top of
the cold -- or unless there is clearly a bacterial infection already.

PLEASE NOTE: As with all of this Web site, I try to give
general answers to common questions my patients and their parents ask me
in my (real) office. If you have specific questions about your
child you must ask your child's regular doctor. No doctor can give
completely accurate advice about a particular child without knowing and
examining that child. I will be happy to try and answer
general questions
about children's health, but unless your child is a regular patient of
mine I cannot give you specific advice.